Bleeding Time (BT) and Clotting Time (CT)

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Bleeding Time Bleeding Time
BLEEDING TIME (BT)

The bleeding time test assesses primary hemostasis (vascular and platelet components) and is dependent on adequate functioning of platelets and blood vessels. In this test, a superficial skin puncture or incision is made and the time required for bleeding to stop is measured. Three methods are commonly used: Duke’s, Ivy’s, and template. Duke’s method, which measures bleeding time following ear lobe puncture, is not advocated since it cannot be standardized and can cause a large local hematoma. In Ivy’s method, 3 punctures are made on the volar surface of the forearm with a lancet (cutting depth 2-2.5 mm) under standardized venous pressure (40 mm Hg). A disadvantage with this method is closure of puncture wound before cessation of bleeding. Template method uses a special surgical blade, which makes a larger cut (5 mm long and 1 mm deep). Although template method is better, it can produce a large scar and even a keloid in predisposed individuals. Ivy’s method is described below.
 
Ivy’s Method
 
Principle
Three standard punctures are made with a lancet on the volar surface of the forearm under standard pressure, and the average time required for bleeding to cease from the puncture sites is measured.
 
Equipment
(1) Sphygmomanometer
(2) Sterile disposable lancets (2-2.5 mm blade with shoulder, which limits the depth of penetration).
(3) Stopwatch
(4) Filter paper
 
Method
(1) A sphygmomanometer cuff is wrapped around the upper arm and inflated to 40 mm of Hg.
(2) The dorsal surface of the forearm is cleansed with 70% ethanol and allowed to dry.
(3) Three punctures are made (about 5 cm apart) in quick succession with a lancet (Superficial veins, and scars or bruises should be avoided).
(4) A stopwatch is started as soon as a puncture is made. One stopwatch is needed for each puncture.
(5) Blood oozing from the puncture wound is gently blotted with a filter paper at 15 seconds intervals. Avoid directly touching the edges of the wound.
(6) The timer is stopped when blood no longer stains the filter paper.
(7) Time required for bleeding to cease from all the three puncture wounds is noted. The average time is reported as the bleeding time.
(8) Sterile adhesive strip is applied over the puncture.
 
Normal Range
2-7 minutes. Majority of individuals have bleeding time less than 4 minutes. It should be reported in minutes or nearest half minute. If bleeding continues beyond 20 minutes, BT should be reported as >20 minutes and the test is discontinued.
 
Causes of prolongation of bleeding time
(1) Thrombocytopenia: If platelet count is less than 1,00,000/ml, bleeding time should not be performed, as it will be prolonged. With a very low platelet count, bleeding may be difficult to control.
(2) Disorders of platelet function
(3) von Willebrand disease
(4) Disorders of blood vessels
 
 
CLOTTING TIME

This is a crude test and is now replaced by activated partial thromboplastin time. Clotting time measures the time required for the blood to clot in a glass test tube kept at 37°C. Prolongation of clotting time only occurs in severe deficiency of a clotting factor and is normal in mild or moderate deficiency.
 
REFERENCES
1. Evatt BL, Gibbs WN, Lewis SM, McArthur JR. Fundamental Diagnostic Hematology: The Bleeding and Clotting Disorders (2nd ed), 1992. US Dept. of health and Human Services, Atlanta, Georgia and World Health Organization, Geneva, Switzerland.
2. Lewis SM, Bain BJ, bates I (Eds). Dacie and Lewis Practical Hematology (9th ed). London: Churchill Livingstone, 2002.
3. Provan D, Krentz A. Oxford Handbook of Clinical and Laboratory Investigations (2002). Oxford university Press. Oxford.
Last modified on Tuesday, 25 July 2017 11:31
Dayyal Dg.

Medical Laboratory Technician at National Institute of Cardiovascular Diseases, Karachi. | Author/Writer/Blogger

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    Figure 862.1 The hypothalamus pituitary ovarian axis
    Figure 862.1 The hypothalamus-pituitary-ovarian axis 
     
    The ovum consists of the secondary oocyte, zona pellucida and corona radiata. The ruptured follicle in the ovary collapses and fills with blood clot (corpus luteum). LH converts granulose cells in the follicle to lutein cells which begin to secrete progesterone. Progesterone stimulates secretion from the endometrial glands (secretory phase) that were earlier under the influence of estrogen. Rising progesterone levels inhibit LH production from the anterior pituitary. Without LH, the corpus luteum regresses and becomes functionless corpus albicans. After regression of corpus luteum, production of estrogen and progesterone stops and endometrium collapses, causing onset of menstruation. If the ovum is fertilized and implanted in the uterine wall, human chorionic gonadotropin (hCG) is secreted by the developing placenta into the maternal circulation. Human chorionic gonadotropin maintains the corpus luteum for secetion of estrogen and progesterone till 12th week of pregnancy. After 12th week, corpus luteum regresses to corpus albicans and the function of synthesis of estrogen and progesterone is taken over by placenta till parturition.
     
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    Figure 862.2 Normal menstrual cycle
    Figure 862.2 Normal menstrual cycle
     
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    Causes of female infertility are shown in Table 862.1.
     
    Table 862.1 Causes of female infertility
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      – Excessive exercise
      – Excess stress
      – Low weight
      – Kallman’s syndrome
      Idiopathic
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      – Hyperprolactinemia
      Hypopituitarism (Sheehan’s syndrome, Simmond’s disease)
      – Craniopharyngioma
      – Cerebral irradiation
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    • Luteinized unruptured follicle
    • Turner’s syndrome
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    • Idiopathic
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      Infections: Tuberculosis, gonorrhea, Chlamydia
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    • Vagina: Septum
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    Evaluation of female infertility is shown in Figure 862.3.
     
    Figure 862.3 Evaluation of female infertility
    Figure 862.3 Evaluation of female infertility. FSH: Follicle stimulating hormone; LH: Luteinizing hormone; DHEA-S: Dihydroepiandrosterone; TSH: Thyroid stimulating hormone; ↑ : Increased; ↓ : Decreased
     
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    Figure 862.4 Ferning of cervical mucosa
    Figure 862.4 Ferning of cervical mucosa
     
    Figure 862.5 Serum progesterone during normal menstrual cycle
    Figure 862.5 Serum progesterone during normal menstrual cycle
     
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    Figure 862.6 Hysterosalpingography
    Figure 862.6 Hysterosalpingography
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    Figure 861.1 Hypothalamus-pituitary-testis axis. + indicates stimulation; – indicates negative feedback
    Figure 861.1 Hypothalamus-pituitary-testis axis. + indicates stimulation; – indicates negative feedback
     
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    Figure 861.2 Steps before and after fertilization of ovum
    Figure 861.2 Steps before and after fertilization of ovum
     
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    Table 861.1 Causes of male infertility 
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    • Endocrine disorders like diabetes mellitus, thyroid dysfunction
    • Genetic disorders: Klinefelter’s syndrome, microdeletions in Y chromosome, autosomal Robertsonian translocation, immotile cilia syndrome (Kartagener’s syndrome), cystic fibrosis, androgen receptor gene defect
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    2. Physical examination: Examination of reproductive system should includes testicular size, undescended testes, hypospadias, scrotal abnormalities (like varicocele), body hair, and facial hair. Varicocele can occur bilaterally and is the most common surgically removable abnormality causing male infertility.
    3. Semen analysis: See article Semen Analysis. Evaluation of azoospermia is shown in Figure 861.3. Evaluation of low semen volume is shown in Figure 861.4.
    4. Chromosomal analysis: This can reveal Klinefelter’s syndrome (e.g. XXY karyotype) (Figure 861.5), deletion in Y chromosome, and autosomal Robertsonian translocation. It is necessary to screen for cystic fibrosis carrier state if bilateral congenital absence of vas deferens is present.
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    Table 861.2 Interpretation of hormonal studies in male infertility 
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    Figure 861.3 Evaluation of azoospermia
    Figure 861.3 Evaluation of azoospermia. FSH: Follicle stimulating hormone; LH: Luteinizing hormone
     
    Figure 861.4 Evaluation of low semen volume
    Figure 861.4 Evaluation of low semen volume
     
    Figure 861.5 Karyotype in Klinefelter's Syndrome
     Figure 861.5 Karyotype in Klinefelter’s syndrome (47, XXY)
     
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  • NORMAL GASTRIC ANATOMY AND PHYSIOLOGY
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    Figure 859.1 Parts of stomach and their lining cells
    Figure 859.1 Parts of stomach and their lining cells 
     
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    • Mucus
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    Figure 859.2 Stimulation of gastric acid secretion
    Figure 859.2 Stimulation of gastric acid secretion. Three receptors on parietal cells stimulate acid secretion: histamine (H2) receptor, acetylcholine or cholinergic receptor, and gastrin/CCK-B receptor. Histamine is released by enterochromaffin-like cells in lamina propria. Acetylcholine is released from nerve endings. Gastrin is released from G cells in antrum (in response to amino acids in food, antral distention, and gastrin-releasing peptide). After binding to receptors, H+ is secreted in exchange for K+ by proton pump

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